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The Structural Basis For The Control Of Cardiac And Skeletal Muscle By The Troponin Complex
Funder
National Health and Medical Research Council
Funding Amount
$369,003.00
Summary
Many key physiological processes are controlled by large, multi-protein complexes. These molecular machines ensure that signals transmitted in the body are correctly interpreted and amplified so as to control key body functions. The Troponin protein complex is one such large multi-protein complex which is the switch used to control both heart and skeletal muscle contraction in the body. The Troponin complex responds to increasing cellular calcium levels, switching the muscle on at high calcium. ....Many key physiological processes are controlled by large, multi-protein complexes. These molecular machines ensure that signals transmitted in the body are correctly interpreted and amplified so as to control key body functions. The Troponin protein complex is one such large multi-protein complex which is the switch used to control both heart and skeletal muscle contraction in the body. The Troponin complex responds to increasing cellular calcium levels, switching the muscle on at high calcium. When calcium returns to its normal basal level, the Troponin complex switches the muscle off. Naturally occurring genetic errors can lead to the malfunction of the Troponin complex. This, in turn, can lead to severe and possibly fatal diseases of the heart and muscle systems. To gain an understanding of these molecular diseases, it is important to understand the structure, dynamics and function of the Troponin complex. This project will use a newly-developed magnetic resonance method to monitor changes in the Troponin structure as a function of calcium level. Each component of the Troponin complex will be labeled with magnetic tags, allowing the determination of both structure and dynamics of Troponin, both in solution and in active muscle fibres. The study will result in a molecular understanding of how the Troponin switch works. This will give great insight in how mutations result in cardiac and muscular diseases.Read moreRead less
Research Fellowship: Protection Of Myocardial Function In Health And Disease
Funder
National Health and Medical Research Council
Funding Amount
$631,010.00
Summary
Heart failure (HF) is a major cause of death in Australia. A/Prof Rebecca Ritchie heads Heart Failure Pharmacology at Baker IDI. Her research focuses on new drug strategies to maintain heart function in response to diabetes & heart attack, common precursors of HF. Many of the treatments discovered from this work are naturally-occurring antioxidants; enhancing their activity will ultimately reduce progression to HF & death in the >3 million Australians affected by these disorders.
Dissecting The Pathogenesis Of The Severe Neurodegenerative Disease, Friedreich’s Ataxia: Development Of Novel Therapeutics
Funder
National Health and Medical Research Council
Funding Amount
$316,449.00
Summary
Friedreich’s ataxia is a devastating neuro- and cardio-degenerative disorder which does not have an effective cure. The studies proposed in this Fellowship are crucial for understanding the progression of this disorder and the development of excitingly new therapeutics.
Diabetic cardiomyopathy (DiabCM) is common in people with diabetes. It predisposes to heat failure. Its cause remains unclear and there is no specific treatment for DiabCM. Inflammation is a fundamental tissue response to a metabolic insult and it occur in DiabCM. The central hypothesis in this work is that inflammation through myocardial macrophage cells contributes to DiabCM. This hypothesis will be tested in animal models and also in cell culutre studies.
Establishing The Intrinsic Regenerative Capacity Of The Adult Human Heart In Health And Disease And The Use Of Recombinant Cellular Growth Factors To Reverse Heart Failure In Vitro
Funder
National Health and Medical Research Council
Funding Amount
$110,615.00
Summary
Heart failure is a major cause of morbidity and mortality in Australia. We hope to change this bleak outlook by showing that the human heart can regenerate, thereby challenging the long-held dogma that our heart cannot regrow. Using human heart samples we will measure the intrinsic capability of these cells to regenerate in heart failure compared to what occurs in normal, healthy ageing. In addition, we will explore the use of extracellular growth factors to stimulate these heart muscle cells
The L-type Calcium Channel As A Reporter Of Successful Morpholino Oligomer Therapy In Treatment Of Duchenne Muscular Dystrophy Cardiomyopathy
Funder
National Health and Medical Research Council
Funding Amount
$595,062.00
Summary
Duchenne Muscular Dystrophy is a fatal muscle wasting disorder. We have previously characterised how the heart fails in a mouse model of muscular dystrophy. We now have preliminary data demonstrating that treatment of mice with morpholino oligomers can rescue cardiac function. This project will fully characterise the effect of the treatment on heart function and optimise therapy regimes with the view to utilising the optimised protocol as a guideline in treating cardiomyopathy in Duchenne Muscul ....Duchenne Muscular Dystrophy is a fatal muscle wasting disorder. We have previously characterised how the heart fails in a mouse model of muscular dystrophy. We now have preliminary data demonstrating that treatment of mice with morpholino oligomers can rescue cardiac function. This project will fully characterise the effect of the treatment on heart function and optimise therapy regimes with the view to utilising the optimised protocol as a guideline in treating cardiomyopathy in Duchenne Muscular Dystrophy boys.Read moreRead less
Molecular And Structural Determinants Of Myocardial Dysfunction And Prognosis In Left And Right Heart Failure.
Funder
National Health and Medical Research Council
Funding Amount
$124,608.00
Summary
The aim of this research is to investigate the role of inherited genetic variation on myocardial function and prognosis in patients with cardiomyopathies as well as pulmonary hypertension. Clinical, cardiac genomic and myocardial tissue studies will be undertaken in various patient cohorts. It is hoped that this research will provide new insights into disease mechanisms, and will contribute to new approaches to patient management and risk stratification.